Endometriosis

Endometriosis is the presence of endometrial glands and stroma outside the endometrial cavity. It presents with cyclical pelvic pain and severe dysmenorrhoea since it is oestrogen and progesterone-sensitive.

• Risk factors
  • Family history
  • Anatomic defects
    • There is increased incidence with obstructive defects
  • Nulliparity
  • Early menarche
  • Late menopause
  • Short menstrual cycle (< 27 days)
  • Longer duration of menstrual flow
  • Menorrhagia (> 1 week)
  • Other environmental factors
    • TCDD/Dioxins (industrial pollutants)
    • Caffeine
    • Alcohol use
• Protective factors
  • Regular exercise
  • High parity
  • Longer duration of lactation
• Pathophysiology
  • Theories
    • Retrograde menstruation: dissemination of endometrial fragments into the peritoneal cavity due to uterine hyperperistalsis/dysperistalsis. This explains endometriosis in women with outflow obstruction.
    • Lymphatic/vascular spread: this is the theory behind its spread into abnormal locations, e.g., retro-orbital
    • Coelomic metaplasia (Meyer’s theroy): suggests that the parietal peritoneum is pluripotent and can transform into endometrial tissue. This explains why some men can get endometriosis.
    • Induction theory: exposure to estrogen induces tranformation of certain tissues into endometrial-like tissue. The ovarian surface epithelium can transform into endometrial like-tissue.
    • Immune dysfunction: this theory isvery complex…
  • Sites of ectopic implantation
    • Dependent areas of the pelvis
      • Anterior and posterior cul-de-sac
      • Uterosacral ligaments
      • Rectovaginal septum
    • Ovary
      • Haemorrhagic cysts known as endometriomas or chocolate cysts.
      • Endometriomas are less likely to produce tosion than other cysts due since they are surrounded by adhesions
    • Bladder
    • Ureters
    • Anterior abdominal wall
    • Diaphragm
  • Regardless of location of endometrial tissue it responds to the normal hormonal cycle resulting in:
    • Production of inflammatory and pain mediators
    • Infertility
    • Nerve dysfunction
  • There is increased prostaglandin and oestrogen formation leading to chronic inflammation (IL 1, IL6, IL 8, TNF alpha all play a role) = PAIN
    • Premenstruation – the tissue is stimulated to grow by progesterone and oestrogen. They enlarge and undergo secretory changes and bleeding.
  • However, surrounding tissues prevent expansion and enlargement of the hemorrhagic fluid causing an increase in pressure = PAIN
  • Severe pain is seen in cases where there are deeply infiltrating lesions.
• Signs and symptoms
  • Pain
    • Cyclical superimposed on chronic
  • Chronic pelvic pain
    • Localized
    • Radiating to the upper back or leg
  • Dysmenorrhoea
    • Pain precedes menses by 24-48 hours
    • Less responsive to NSAIDs and combined oral contraceptives
  • Dyspareunia
    • This is partly caused by implants in the uterosacral ligament
  • Dysuria
    • This is associated with cyclical frequency and urgency
  • Defecatory pain
  • Infertility or subfertility
    • This occurs when the implants disrupt tubo-ovarian structures or implant in the ovaries
  • Symptoms of intestinal obstruction
  • Symptoms of urethral obstruction
• Physical exam
  • Blue or powder-burn red lesions which bleed easily can sometimes be seen on speculum exam
  • Uterosacral ligament nodularity and tenderness
  • Fixed, tender and retroverted uterus
  • Palpable (enlarged) cystic adnexal mass
  • Fixed, firm posterior cul-de-sac
• Differentials
  • Pelvic inflammatory disease
  • Hemorrhagic ovarian cyst
  • Ovarian torsion
  • Primary dysmenorrhea
  • Degenerating leiomyoma
  • Ectopic pregnancy
• Investigations
  • Transvaginal ultrasound to identify endometriomas
    • The uterus is generally not enlarged
    • An endometrioma appears as a homogenous cystic lesion with ground-glass internal echos, which surround a normal-appearing ovarian stroma
    • Nodules
  • CT-scan or MRI
  • Diagnostic laparoscopy + biopsy for definitive diagnosis
    • Endometrial glands and stroma outside the endometrial cavity
    • Red lesions
    • White/clear implants
    • Black-brown “powder-burn” lesions
    • Endometriomas (brown-black cystic lesions of the ovary classically filled with chocolate-colored fluid)
  • Complete blood count
  • Urine hCG
  • Urinalysis + culture
  • Vaginal/Cervical culture
• Treatment
  • NSAIDS (ibruprofen or naproxen) for primary dysmenorrhoea and pelvic pain prior to laparoscopic diagnosis or confirmed endometriosis with mild symptoms
  • Combined oral contraceptives (COCs) to reduce endometriorsis-related pain
  • Progestins for patients with contraindications to oestrogens
    • Depot medroxyprogesterone acetate (DMPA) can reduce bone mineral density
    • Norethindrone acetate is very effective with Leuprolide
    • Levonorgestrel-intrauterine system
    • Ulipristal acetate(Ella)
    • Mifepristone (off-label)
    • Norethisterone
  • Androgens (danazol or gestrinone)
    • These have a significant adverse effect profile
  • GnRH agonists (leuprolide, goserelin, or nafarelin)
    • These decrease pituitary GnRH production and downstream ovarian estrogen production.
    • An initial gonadotropin surge may worsen symptoms for 1-2 weeks before improvment.
    • Add-back therapy (low-dose estrogen and progestin supplementation) may be required to minimize hypoestrogenic and osteoporotic side effects
  • Aromatase inhibitors (anastrozole, or letrozole)
  • Surgery is the definitive treatment
    • Lesion ablation with adhesiolysis
    • Endometrioma resection
    • Presacral neurectomy
    • Cystectomy is preferred over cyst aspiration for endometriomas
    • Bilateral salpingo-oophorectomy for persistent symptoms despite medical treatment and previous surgery
    • Hysterectomy with bilateral salpingoophorectomy is the most definitive surgical treatment. It is considered in women who do not wish to preserve fertility